When people suffer from diabetes, their fasting blood glucose levels reach 126 mg/dL or more. Even if fasting blood glucose levels fall within a normal range, some people exhibit postprandial blood glucose levels as high as 140 to 200 mg/dL and are diagnosed as having impaired glucose tolerance (hereinafter referred to as IGT). It has been considered that the risk of cardiovascular disorders can be reduced by delaying the onset of diabetes from IGT, and several supportive findings for this have been obtained. For example, the Da Qing IGT and Diabetes Study carried out in China in 1997 has reported that progression of IGT into Type II diabetes is significantly suppressed by diet and exercise (see Non-patent Document 1). As a case where medication is effective, an α-glucosidase inhibitor, acarbose, which inhibits sugar hydrolases to delay sugar absorption from the small intestine has been reported to suppress the development of Type II diabetes from IGT and further significantly suppress the onset of hypertension (see Non-patent Document 2).
In view of the foregoing, to suppress the onset of diabetes, it is important to control IGT by diet therapy, exercise therapy and medication.
Nevertheless, when people suffer from diabetes, it comes to be necessary to control their blood glucose levels at all times. Diabetes is basically treated by diet therapy and exercise therapy; however, when sufficient effect is not obtained by these therapies, medication must be chosen.
On the mammalian small intestinal epithelium, sodium-dependent glucose transporter 1 (SGLT1) is expressed at a high frequency. It is known that SGLT1 serves depending upon sodium and plays a role in active transport of glucose or galactose in the small intestine. Therefore, if glucose taken from a meal can be suppressed, IGT may be prevented or treated. Based on this concept, pyrazole derivatives inhibiting SGLT1 activity have been reported (see Patent Documents 1 to 6).
Furthermore, sodium-dependent glucose transporter 2 (SGLT2) is expressed at a high frequency in the kidney. Glucose once filtered by the glomeruli is reabsorbed via SGLT2 (see Non-patent Document 3). When an SGLT2 inhibitor is administered to diabetic rats, sugar excretion into urine is facilitated to induce a hypoglycemic action. From this, an SGLT2-specific inhibitor has been considered as a target molecule serving as a novel therapeutic agent for diabetes (see Non-patent Document 4). In these circumstances, studies have been conducted on SGLT2 inhibitors, and various types of O-aryl glycoside derivatives have been provided (see Patent Documents 7 and 8).
Accordingly, if SGLT1 and SGLT2 activities can be inhibited simultaneously, a novel type of therapeutic agent for diabetes can be provided, which has not only postprandial hyperglycemia suppression action ascribed to SGLT1 inhibition but also progressive hypoglycemic action ascribed to SGLT2 inhibition.
Up to now, C-phenyl glucitol derivatives with selective inhibitory activity against SGLT2 have been reported (see Patent Document 9); however, C-phenyl 1-thioglucitol derivatives strongly inhibiting both SGLT1 and SGLT2 have not yet been reported.    Patent Document 1: International Publication No. WO2002/098893    Patent Document 2: International Publication No. WO2004/014932    Patent Document 3: International Publication No. WO2004/018491    Patent Document 4: International Publication No. WO2004/019958    Patent Document 5: International Publication No. WO2005/121161    Patent Document 6: International Publication No. WO2004/050122    Patent Document 7: European Patent Publication No. 0850948    Patent Document 8: International Publication No. WO2001/068660    Patent Document 9: International Publication No. WO2001/027128    Non-patent Document 1: Pan X R, et al. Diabets Care, vol. 20, p. 534, 1997    Non-patent Document 2: J.-L. Chiasson, et al. Lancent, vol. 359, p. 2072, 2002    Non-patent Document 3: E. M. Wright, Am. J. Physiol. Renal. Physiol., vol. 280, p. F10, 2001    Non-patent Document 4: G. Toggenburger, et al. Biochem. Biophys. Acta., vol. 688, p. 557, 1982